Lcorl, or ligand-dependent corepressor-like, is a gene strongly associated with metabolic traits, especially body size, glucose homeostasis, and growth in humans and livestock [1,2,3,4,5,6,7,8]. Genome-wide association studies (GWAS) have identified it as a key locus related to these characteristics, yet its functional mechanisms were unclear until detailed research was carried out [1].

In Lcorl knockout mice (Lcorl-/-), the pups are born smaller, but reach normal weight by 7-9 weeks. As they age, these mice remain lean with decreased daily food intake. Their glucose tolerance and insulin sensitivity are improved. Mechanistically, the stunted growth is linked to reduced circulating IGF-1 levels, and the expression of genes downstream of GH signaling, as well as those involved in glucose and lipid metabolism, are altered in the liver. Also, Lcorl-/-mice are protected against high-fat diet challenges but show reduced exercise capacity [1].

In conclusion, Lcorl plays a crucial role in regulating growth and metabolism. The Lcorl knockout mouse model has been instrumental in revealing its function in growth, body weight regulation, glucose homeostasis, and response to diet challenges, providing valuable insights into the gene's role in metabolic-related processes and potentially related diseases [1].